Heart Arrest, Out-Of-HospitalPhase 2NCT04563000
Impact of Vitamin C on Biomarkers of Neurologic Injury in Survivors of Cardiac Arrest
A Phase 2 study testing Vitamin C in people with Heart Arrest, Out-Of-Hospital and Biomarkers, run by University Medical Centre Maribor at 1 site in Slovenia.
Trial summary
Out-of-hospital cardiac arrest (OHCA) is one of the leading cause of death in the world. In Slovenia approximately 25% of resuscitated patients survives to discharge from hospitals, usually with poorer functional status. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Heart Arrest, Out-Of-Hospital, Biomarkers, Oxidative Stress
- What is being tested?
- Vitamin C
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 150 participants
- Where
- 1 siteSlovenia
- Study dates
- 1 Oct 2020to 31 Dec 2022
- Phase
- Phase 2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- comatose survivors of out-of-hospital arrest
Who cannot join
- patients with trauma, asphyxia, drowning or electrocution as a cause of cardiac arrest
- history of oxalate nephropathy or nephrolithiasis, glucose-6-phosphate dehydrogenase deficiency, and hemochromatosis
- pregnancy
Trial locations and contacts
1 site in 1 country.
Slovenia1 site
University Medical Centre Maribor
Maribor, 2000
Andrej Markota, MD, PhD, Assist. Prof., +38651311519, andrej.markota@ukc-mb.si
Matevž Privšek, MD, +38640642986, matevz.privsek@icloud.com
About this study
Official title: Impact of Vitamin C on Biomarkers of Neurologic Injury in Patients With Return of Spontaneous Circulation After Out-of-Hospital Cardiac Arrest
Out-of-hospital cardiac arrest (OHCA) is one of the leading cause of death in the world. In Slovenia approximately 25% of resuscitated patients survives to discharge from hospitals, usually with poorer functional status.
One of key pathophysiological process responsible for poorer functional status is global hypoxic-ischemic injury, which is two-stage. Primary stage occurs immediately after cardiac arrest due to cessation of blood flow. With return of spontaneous circulation a secondary injury occurs, of which the leading process is an imbalance between oxygen delivery and consumption. Reperfusion exposes ischemic tissue to oxygen, resulting in the formation of large amounts of highly reactive oxygen species (ROS) within minutes. ROS lead to oxidative stress, which causes extensive damage to cell structures and leads to cell death. Consequently, necrosis and apoptosis are responsible for organ dysfunction and functional outcome of these patients.
Read more
Such injury of neural tissue causes brain damage, which is ultimately responsible for poor neurological and thus functional outcome of OHCA survivors. The extent of brain damage can be determined in several ways: clinically by assessing quantitative and qualitative consciousness and the presence of involuntary movements in an unconscious patient, by assessing activity on electroencephalographic record, by imaging of the brain with computed tomography and magnetic resonance imaging, as well as by assessing levels of biological markers of brain injury. Of the latter, the S-100b protein and neuron-specific enolase have been shown to be suitable for such assessment.
Oxidative stress is counteracted by the body with endogenous antioxidants that balance excess free radicals and stabilize cellular function. Vitamin C (ascorbic acid) is the body's main antioxidant and is primarily consumed during oxidative stress. Large amounts of ROS rapidly depletes the body's vitamin C stores.
Humans cannot synthesise vitamin C and enteral uptake of vitamin C is limited by transporter saturation. On the other hand, parenteral (venous) dosing of vitamin C can achieve concentrations of vitamin C above physiological and thus produce a stronger antioxidant effect. The beneficial effect of parenteral dosing of vitamin C has been establish in several preclinical and clinical studies in patients with ischemic stroke and cardiac arrest.
The investigators hypothesize that there is a similarly beneficial effect of vitamin C in survivors of OHCA.
- Being tested
- Vitamin C, Placebo
- Keywords
- vitamin C, biomarkers, brain injury, cardiac arrest
- Medical subject headings
- Out-of-Hospital Cardiac Arrest, Trauma, Nervous System, Brain Injuries, Heart Arrest
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Vitamin CDrug
Ascorbic acid 1,5 g intravenously every 12-hours for 4 consecutive days
PlaceboDrug
0,9 % solution of sodium chloride 100 ml intravenously every 12-hours for 4 consecutive days
| Study group | Role | What they receive |
|---|---|---|
| Vitamin C | Experimental | Group of patients that will receive vitamin C (ascorbic acid 1,5 g mixed with 0,9 % solution of sodium chloride 100 ml every 12 hours for 4 days intravenously). Receives: Drug: Vitamin C |
| Placebo | Placebo comparator | Group of patients that will receive placebo (0,9 % solution of sodium chloride 100 ml every 12 hours for 4 days intravenously). Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Biomarkers of neurological injury
Serum levels of protein S-100b and neuron-specific enolase.
Measured: 5th day
Secondary outcomes (19)
Brain imaging (CT and MRI)
Unconscious survivors will have first brain imaging on the 3rd day, if still unconscious, second imaging around the 10th day. Imaging results will be descriptive (normal or pathological with signs of global ischemic injury: generalised edema, reduced grey and white matter differentiation, obliteration of the sulci). Second image will be compared to the first.
Measured: 3rd-10th day
Electroencephalography (EEG)
Unconscious survivors will have first EEG on the 3rd day, if still unconscious, second imaging around the 10th day. EEG results will be descriptive (normal or pathological with background suppression with or without periods of bursts, with or without response to external stimulus and similar patterns). Second EEG will be compared to the first.
Measured: 3rd-10th day
Evaluation of pupils
Pupils size, reactivity and symmetry on admission and during hospitalisation will be observed daily.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of involuntary movements
The presence of involuntary movements will be observed daily.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of GCS
Level of consciousness will be determined daily with Glasgow Coma Scale (GCS).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of FOUR
Level of consciousness will be determined daily with Full Outline of UnResponsiveness (FOUR) score.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Cerebral Performance Category
Cerebral Performance Category (CPC) at discharge will be recorded.
Measured: from admission till discharge from ICU or death (whatever comes first)
Left ventricular ejection fraction
Left ventricular ejection fraction (first, last, best, worst), determined by ultrasound will be noted.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Arrhythmias
Presence of arrhythmias and the need for treating them will be recorded.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of heart failure
Clinical evaluation of heart failure according to Killip-Kimball classification will be performed (worst result).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum troponin level
Serum troponin levels will be determined (on admission, minimal, maximal).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum Brain natriuretic peptide
Serum brain natriuretic peptide levels will be determined (on admission, minimal, maximal).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Vasopressor and/or inotrope need
The need for vasopressors and inotropes will be noted, along with the name of the substance, maximal dosage and duration.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Mechanical ventilation
Days and hours of mechanical ventilation will be noted.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Kidney failure
The need for renal replacement therapy (and consecutive day of such therapy) will be recorded.
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum urea levels
Serum levels of urea will be recorded (on admission, minimal, maximal).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum creatinine levels
Serum creatinine levels will be recorded (on admission, minimal, maximal).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum C-reactive protein levels
Serum C-reactive protein levels will be determined (on admission, minimal, maximal).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum procalcitonin levels
Serum procalcitonin levels will be determined (on admission, minimal, maximal).
Measured: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted24 Sep 2020
- Study start1 Oct 2020 (estimated)
- Primary completion31 Oct 2022 (estimated)
- Study completion31 Dec 2022 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (17)Papers the sponsor has linked to this study.
- Other trials for Heart Arrest, Out-Of-HospitalStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind
- Who is masked
- Participant, Care provider, Outcomes assessor
- Enrolment
- 150 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University Medical Centre Maribor
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Andrej Markota, MD, PhD, Assist. Prof., Study chair, University Medical Centre Maribor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04563000
- Sponsor's protocol ID
- VitC
- Status last verified
- Sep 2020
- First submitted
- 10 Sep 2020
- Last updated
- 24 Sep 2020
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Grasner JT, Lefering R, Koster RW, Masterson S, Bottiger BW, Herlitz J, Wnent J, Tjelmeland IB, Ortiz FR, Maurer H, Baubin M, Mols P, Hadzibegovic I, Ioannides M, Skulec R, Wissenberg M, Salo A, Hubert H, Nikolaou NI, Loczi G, Svavarsdottir H, Semeraro F, Wright PJ, Clarens C, Pijls R, Cebula G, Correia VG, Cimpoesu D, Raffay V, Trenkler S, Markota A, Stromsoe A, Burkart R, Perkins GD, Bossaert LL; EuReCa ONE Collaborators. EuReCa ONE-27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation. 2016 Aug;105:188-95. doi: 10.1016/j.resuscitation.2016.06.004. Epub 2016 Jun 16.
PubMed 27321577Nolan JP, Neumar RW, Adrie C, Aibiki M, Berg RA, Bottiger BW, Callaway C, Clark RS, Geocadin RG, Jauch EC, Kern KB, Laurent I, Longstreth WT, Merchant RM, Morley P, Morrison LJ, Nadkarni V, Peberdy MA, Rivers EP, Rodriguez-Nunez A, Sellke FW, Spaulding C, Sunde K, Hoek TV. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke. Resuscitation. 2008 Dec;79(3):350-79. doi: 10.1016/j.resuscitation.2008.09.017. Epub 2008 Oct 28.
PubMed 18963350Sekhon MS, Ainslie PN, Griesdale DE. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a "two-hit" model. Crit Care. 2017 Apr 13;21(1):90. doi: 10.1186/s13054-017-1670-9.
PubMed 28403909Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) [RETIRED]: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006 Jul 25;67(2):203-10. doi: 10.1212/01.wnl.0000227183.21314.cd.
PubMed 16864809Calderon LM, Guyette FX, Doshi AA, Callaway CW, Rittenberger JC; Post Cardiac Arrest Service. Combining NSE and S100B with clinical examination findings to predict survival after resuscitation from cardiac arrest. Resuscitation. 2014 Aug;85(8):1025-9. doi: 10.1016/j.resuscitation.2014.04.020. Epub 2014 Apr 30.
PubMed 24795283Shinozaki K, Oda S, Sadahiro T, Nakamura M, Abe R, Nakada TA, Nomura F, Nakanishi K, Kitamura N, Hirasawa H. Serum S-100B is superior to neuron-specific enolase as an early prognostic biomarker for neurological outcome following cardiopulmonary resuscitation. Resuscitation. 2009 Aug;80(8):870-5. doi: 10.1016/j.resuscitation.2009.05.005. Epub 2009 Jun 17.
PubMed 19535196Spoelstra-de Man AME, Elbers PWG, Oudemans-van Straaten HM. Making sense of early high-dose intravenous vitamin C in ischemia/reperfusion injury. Crit Care. 2018 Mar 20;22(1):70. doi: 10.1186/s13054-018-1996-y.
PubMed 29558975Levine M, Padayatty SJ, Espey MG. Vitamin C: a concentration-function approach yields pharmacology and therapeutic discoveries. Adv Nutr. 2011 Mar;2(2):78-88. doi: 10.3945/an.110.000109. Epub 2011 Mar 10.
PubMed 22332036Tsai MS, Huang CH, Tsai CY, Chen HW, Lee HC, Cheng HJ, Hsu CY, Wang TD, Chang WT, Chen WJ. Ascorbic acid mitigates the myocardial injury after cardiac arrest and electrical shock. Intensive Care Med. 2011 Dec;37(12):2033-40. doi: 10.1007/s00134-011-2362-6. Epub 2011 Sep 28.
PubMed 21953354Tsai MS, Huang CH, Tsai CY, Chen HW, Cheng HJ, Hsu CY, Chang WT, Chen WJ. Combination of intravenous ascorbic acid administration and hypothermia after resuscitation improves myocardial function and survival in a ventricular fibrillation cardiac arrest model in the rat. Acad Emerg Med. 2014 Mar;21(3):257-65. doi: 10.1111/acem.12335.
PubMed 24628750Gao F, Yao CL, Gao E, Mo QZ, Yan WL, McLaughlin R, Lopez BL, Christopher TA, Ma XL. Enhancement of glutathione cardioprotection by ascorbic acid in myocardial reperfusion injury. J Pharmacol Exp Ther. 2002 May;301(2):543-50. doi: 10.1124/jpet.301.2.543.
PubMed 11961055Nishinaka Y, Sugiyama S, Yokota M, Saito H, Ozawa T. The effects of a high dose of ascorbate on ischemia-reperfusion-induced mitochondrial dysfunction in canine hearts. Heart Vessels. 1992;7(1):18-23. doi: 10.1007/BF01745863.
PubMed 1583008Basili S, Tanzilli G, Mangieri E, Raparelli V, Di Santo S, Pignatelli P, Violi F. Intravenous ascorbic acid infusion improves myocardial perfusion grade during elective percutaneous coronary intervention: relationship with oxidative stress markers. JACC Cardiovasc Interv. 2010 Feb;3(2):221-9. doi: 10.1016/j.jcin.2009.10.025.
PubMed 20170881Dingchao H, Zhiduan Q, Liye H, Xiaodong F. The protective effects of high-dose ascorbic acid on myocardium against reperfusion injury during and after cardiopulmonary bypass. Thorac Cardiovasc Surg. 1994 Oct;42(5):276-8. doi: 10.1055/s-2007-1016504.
PubMed 7863489Henry PT, Chandy MJ. Effect of ascorbic acid on infarct size in experimental focal cerebral ischaemia and reperfusion in a primate model. Acta Neurochir (Wien). 1998;140(9):977-80. doi: 10.1007/s007010050201.
PubMed 9842436
Study at a glance
From the registry record, last updated by the sponsor on 24 Sep 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Impact of Vitamin C on Biomarkers of Neurologic Injury in Patients With Return of Spontaneous Circulation After Out-of-Hospital Cardiac Arrest
- ClinicalTrials.gov ID
- NCT04563000
- Acronym / sponsor ID
- VitC
- Keywords
- vitamin C, biomarkers, brain injury, cardiac arrest
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 150 participants (estimated)
- Lead sponsor
- University Medical Centre MariborUniversity, hospital or other
- Study start
- 1 Oct 2020 (estimated)
- Primary completion
- 31 Oct 2022 (estimated)
- Study completion
- 31 Dec 2022 (estimated)
- First posted
- 24 Sep 2020 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Out-of-hospital cardiac arrest (OHCA) is one of the leading cause of death in the world. In Slovenia approximately 25% of resuscitated patients survives to discharge from hospitals, usually with poorer functional status.
One of key pathophysiological process responsible for poorer functional status is global hypoxic-ischemic injury, which is two-stage. Primary stage occurs immediately after cardiac arrest due to cessation of blood flow. With return of spontaneous circulation a secondary injury occurs, of which the leading process is an imbalance between oxygen delivery and consumption. Reperfusion exposes ischemic tissue to oxygen, resulting in the formation of large amounts of highly reactive oxygen species (ROS) within minutes. ROS lead to oxidative stress, which causes extensive damage to cell structures and leads to cell death. Consequently, necrosis and apoptosis are responsible for organ dysfunction and functional outcome of these patients.
Such injury of neural tissue causes brain damage, which is ultimately responsible for poor neurological and thus functional outcome of OHCA survivors. The extent of brain damage can be determined in several ways: clinically by assessing quantitative and qualitative consciousness and the presence of involuntary movements in an unconscious patient, by assessing activity on electroencephalographic record, by imaging of the brain with computed tomography and magnetic resonance imaging, as well as by assessing levels of biological markers of brain injury. Of the latter, the S-100b protein and neuron-specific enolase have been shown to be suitable for such assessment.
Oxidative stress is counteracted by the body with endogenous antioxidants that balance excess free radicals and stabilize cellular function. Vitamin C (ascorbic acid) is the body's main antioxidant and is primarily consumed during oxidative stress. Large amounts of ROS rapidly depletes the body's vitamin C stores.
Humans cannot synthesise vitamin C and enteral uptake of vitamin C is limited by transporter saturation. On the other hand, parenteral (venous) dosing of vitamin C can achieve concentrations of vitamin C above physiological and thus produce a stronger antioxidant effect. The beneficial effect of parenteral dosing of vitamin C has been establish in several preclinical and clinical studies in patients with ischemic stroke and cardiac arrest.
The investigators hypothesize that there is a similarly beneficial effect of vitamin C in survivors of OHCA.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind (participant, care provider, outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Vitamin C | Experimental | Drug: Vitamin CGroup of patients that will receive vitamin C (ascorbic acid 1,5 g mixed with 0,9 % solution of sodium chloride 100 ml every 12 hours for 4 days intravenously). |
| Placebo | Placebo comparator | Drug: PlaceboGroup of patients that will receive placebo (0,9 % solution of sodium chloride 100 ml every 12 hours for 4 days intravenously). |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (1 listed)
- comatose survivors of out-of-hospital arrest
Key exclusion criteria (3 listed)
- patients with trauma, asphyxia, drowning or electrocution as a cause of cardiac arrest
- history of oxalate nephropathy or nephrolithiasis, glucose-6-phosphate dehydrogenase deficiency, and hemochromatosis
- pregnancy
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Vitamin CAscorbic acid 1,5 g intravenously every 12-hours for 4 consecutive days | Drug | Vitamin C |
| Placebo0,9 % solution of sodium chloride 100 ml intravenously every 12-hours for 4 consecutive days | Drug | Placebo |
Primary outcome
Biomarkers of neurological injury
Time frame: 5th day
Serum levels of protein S-100b and neuron-specific enolase.
19 secondary outcomes
Brain imaging (CT and MRI)
Time frame: 3rd-10th day
Electroencephalography (EEG)
Time frame: 3rd-10th day
Evaluation of pupils
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of involuntary movements
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of GCS
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of FOUR
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Cerebral Performance Category
Time frame: from admission till discharge from ICU or death (whatever comes first)
Left ventricular ejection fraction
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Arrhythmias
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Evaluation of heart failure
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum troponin level
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum Brain natriuretic peptide
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Vasopressor and/or inotrope need
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Mechanical ventilation
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Kidney failure
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum urea levels
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum creatinine levels
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum C-reactive protein levels
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Serum procalcitonin levels
Time frame: from admission until 14 days or till discharge from ICU or death (whatever comes first)
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 24 Sep 2020.
- Background: PubMed 27321577Grasner JT, Lefering R, Koster RW, Masterson S, Bottiger BW, Herlitz J, Wnent J, Tjelmeland IB, Ortiz FR, Maurer H, Baubin M, Mols P, Hadzibegovic I, Ioannides M, Skulec R, Wissenberg M, Salo A, Hubert H, Nikolaou NI, Loczi G, Svavarsdottir H, Semeraro F, Wright PJ, Clarens C, Pijls R, Cebula G, Correia VG, Cimpoesu D, Raffay V, Trenkler S, Markota A, Stromsoe A, Burkart R, Perkins GD, Bossaert LL; EuReCa ONE Collaborators. EuReCa ONE-27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation. 2016 Aug;105:188-95. doi: 10.1016/j.resuscitation.2016.06.004. Epub 2016 Jun 16.
- Background: PubMed 18963350Nolan JP, Neumar RW, Adrie C, Aibiki M, Berg RA, Bottiger BW, Callaway C, Clark RS, Geocadin RG, Jauch EC, Kern KB, Laurent I, Longstreth WT, Merchant RM, Morley P, Morrison LJ, Nadkarni V, Peberdy MA, Rivers EP, Rodriguez-Nunez A, Sellke FW, Spaulding C, Sunde K, Hoek TV. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke. Resuscitation. 2008 Dec;79(3):350-79. doi: 10.1016/j.resuscitation.2008.09.017. Epub 2008 Oct 28.
- Background: PubMed 28403909Sekhon MS, Ainslie PN, Griesdale DE. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a "two-hit" model. Crit Care. 2017 Apr 13;21(1):90. doi: 10.1186/s13054-017-1670-9.
- Background: PubMed 16864809Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) [RETIRED]: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006 Jul 25;67(2):203-10. doi: 10.1212/01.wnl.0000227183.21314.cd.
- Background: PubMed 24795283Calderon LM, Guyette FX, Doshi AA, Callaway CW, Rittenberger JC; Post Cardiac Arrest Service. Combining NSE and S100B with clinical examination findings to predict survival after resuscitation from cardiac arrest. Resuscitation. 2014 Aug;85(8):1025-9. doi: 10.1016/j.resuscitation.2014.04.020. Epub 2014 Apr 30.
- Background: PubMed 19535196Shinozaki K, Oda S, Sadahiro T, Nakamura M, Abe R, Nakada TA, Nomura F, Nakanishi K, Kitamura N, Hirasawa H. Serum S-100B is superior to neuron-specific enolase as an early prognostic biomarker for neurological outcome following cardiopulmonary resuscitation. Resuscitation. 2009 Aug;80(8):870-5. doi: 10.1016/j.resuscitation.2009.05.005. Epub 2009 Jun 17.
- Background: PubMed 29558975Spoelstra-de Man AME, Elbers PWG, Oudemans-van Straaten HM. Making sense of early high-dose intravenous vitamin C in ischemia/reperfusion injury. Crit Care. 2018 Mar 20;22(1):70. doi: 10.1186/s13054-018-1996-y.
- Background: PubMed 22332036Levine M, Padayatty SJ, Espey MG. Vitamin C: a concentration-function approach yields pharmacology and therapeutic discoveries. Adv Nutr. 2011 Mar;2(2):78-88. doi: 10.3945/an.110.000109. Epub 2011 Mar 10.
- Background: PubMed 21953354Tsai MS, Huang CH, Tsai CY, Chen HW, Lee HC, Cheng HJ, Hsu CY, Wang TD, Chang WT, Chen WJ. Ascorbic acid mitigates the myocardial injury after cardiac arrest and electrical shock. Intensive Care Med. 2011 Dec;37(12):2033-40. doi: 10.1007/s00134-011-2362-6. Epub 2011 Sep 28.
- Background: PubMed 24628750Tsai MS, Huang CH, Tsai CY, Chen HW, Cheng HJ, Hsu CY, Chang WT, Chen WJ. Combination of intravenous ascorbic acid administration and hypothermia after resuscitation improves myocardial function and survival in a ventricular fibrillation cardiac arrest model in the rat. Acad Emerg Med. 2014 Mar;21(3):257-65. doi: 10.1111/acem.12335.
- Background: PubMed 11961055Gao F, Yao CL, Gao E, Mo QZ, Yan WL, McLaughlin R, Lopez BL, Christopher TA, Ma XL. Enhancement of glutathione cardioprotection by ascorbic acid in myocardial reperfusion injury. J Pharmacol Exp Ther. 2002 May;301(2):543-50. doi: 10.1124/jpet.301.2.543.
- Background: PubMed 1583008Nishinaka Y, Sugiyama S, Yokota M, Saito H, Ozawa T. The effects of a high dose of ascorbate on ischemia-reperfusion-induced mitochondrial dysfunction in canine hearts. Heart Vessels. 1992;7(1):18-23. doi: 10.1007/BF01745863.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Andrej Markota, MD, PhD, Assist. Prof. study chair
University Medical Centre Maribor
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Vitamin C in people with Heart Arrest, Out-Of-Hospital and Biomarkers, run by University Medical Centre Maribor at 1 site in Slovenia.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 24 Sep 2020. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Slovenia. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Andrej Markota, MD, PhD, Assist. Prof. (+38651311519, andrej.markota@ukc-mb.si), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Biomarkers of neurological injury (time frame: 5th day). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT04563000, which also lists 17 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 24 Sep 2020.